ArticleInternational journal of cancer2013
Doxorubicin sensitizes human tumor cells to NK cell- and T-cell-mediated killing by augmented TRAIL receptor signaling.
Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- Multifaced Anticancer Potential of Doxorubicin: Spotlight on Breast Cancer.Diseases & research · 2025Article
- Construction of anti-HER2 affibody-directed CAR-NK and its synergistic effects with doxorubicin-loaded nanodrug against HER2-positive breast cancer.Frontiers in immunology · 2025Article
- Pan-cancer analysis of T-cell proliferation regulatory genes as potential immunotherapeutic targets.Aging · 2024Article
- Impact of doxorubicin-loaded ferritin nanocages (FerOX) vs. free doxorubicin on T lymphocytes: a translational clinical study on breast cancer patients undergoing neoadjuvant chemotherapy.Journal of nanobiotechnology · 2024Article
- Characterizing influence of rCHOP treatment on diffuse large B-cell lymphoma microenvironment through in vitro microfluidic spheroid model.Cell death & disease · 2024Article
- Cellular immunity analysis by a modular acoustofluidic platform: CIAMAP.Science advances · 2023Article
- Apoptosis: aJournal for immunotherapy of cancer · 2023Review
- Harnessing novel strategies and cell types to overcome immune tolerance during adoptive cell therapy in cancer.Journal for immunotherapy of cancer · 2023Review
- Effects of Leea indica leaf extracts and its phytoconstituents on natural killer cell-mediated cytotoxicity in human ovarian cancer.BMC complementary medicine and therapies · 2023Article
- Genistein Sensitizes Human Cholangiocarcinoma Cell Lines to Be Susceptible to Natural Killer Cells.Biology · 2022Article
- Doxorubicin sensitizes breast cancer cells to natural killer cells in connection with increased Fas receptors.International journal of molecular medicine · 2022Article
- The Biological Role and Therapeutic Potential of NK Cells in Hematological and Solid Tumors.International journal of molecular sciences · 2021Review
- Natural Killer Cells and Anti-Cancer Therapies: Reciprocal Effects on Immune Function and Therapeutic Response.Cancers · 2021Review
- Dissecting pharmacological effects of chloroquine in cancer treatment: interference with inflammatory signaling pathways.Immunology · 2020Review
- Tumor Microenvironment following Gemcitabine Treatment Favors Differentiation of Immunosuppressive Ly6CJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Interferon β and Anti-PD-1/PD-L1 Checkpoint Blockade Cooperate in NK Cell-Mediated Killing of Nasopharyngeal Carcinoma Cells.Translational oncology · 2019Article
- Review
- Telomerase reverse transcriptase interference synergistically promotes tumor necrosis factor‑related apoptosis‑inducing ligand‑induced oral squamous cell carcinoma apoptosis and suppresses proliferation in vitro and in vivo.International journal of molecular medicine · 2018Article
- Chemo-photothermal therapy combination elicits anti-tumor immunity against advanced metastatic cancer.Nature communications · 2018Article
- IFN-γ orchestrates tumor elimination, tumor dormancy, tumor escape, and progression.Journal of leukocyte biology · 2018Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Doxorubicin (DOX) is an anthracycline antibiotic that is widely used to treat different types of malignancy. In this study, it was studied whether DOX could be used to render tumor cells susceptible to apoptosis by NK and T cells. Pretreatment with subapoptotic doses of DOX sensitized tumor cell lines of various histotypes to both NK and T cells resulting in a 3.7 to 32.7% increase in lysis (2.5 mean fold increase, p < 0.0001) and a 2.9 to 14.2% increase in lysis (3.0 mean-fold increase, p < 0.05), respectively. The sensitizing effect of the drug was primarily dependent on the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/TRAIL-receptor signaling, but not on Fas-ligand, perforin, NKG2D or DNAM-1. The central role of the TRAIL signaling pathway was further supported by an increased expression of TRAIL-R2 on DOX-treated tumor cells and by downregulation of cellular FLICE inhibitory protein, the inhibitors of death receptor-mediated apoptosis. Compared to untreated cells, pretreatment of tumor cells with DOX showed increased processing and activation of caspase-8 on coculture with NK or T cells. The significance of this treatment strategy was confirmed using a xenogeneic tumor-bearing mouse model. Tumor progression was delayed in mice that received either NK cells (p < 0.05) or T cells (p < 0.0001) following DOX treatment compared to mice receiving either cell type alone. Moreover, combined infusion of both NK and T cells following DOX treatment not only delayed tumor progression but also significantly improved the long-term survival (p < 0.01). Based on these findings, it was proposed that DOX can be used to improve the efficacy of adoptive cell therapy in patients with cancer.
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